The research proposed here is concerned with the mechanism of permeation of toxic gaseous impurities (e.g., NO2, SO, O3 and others) in air from the lung into the bloodstream. Particular attention will be directed to adverse effects these contaminants may have on lung permeation capacity, structural changes in the cell walls and on the mechanism of permeation in general. The bimolecular lipid membrane, BLM, will be taken as model for cell membranes or cell walls. The BLM is recognized as an universal model for human cell membranes, whose properties closely resemble those of natural membranes. One of the initial steps after inhalation of air is its dissolution in the aqueous phase of the respective system (i.e., alveoli) and its subsequent deeper penetration through the lung cell walls and blood capillary walls into the bloodstream. This mechanism is understood to a certain extent in the case of pure air but not at all as far as toxic impurities of air are concerned. The research proposed here will constitute a study of the mode of action of such impurities during permeation of the respective walls and of their adverse effects reducing or incapacitating the proper function of such cell walls. Techniques for the formation of various BLMs and for measuring their permeabilities are now well established (e.g., diffusion by osmotic flow or also passive permeability). The BLM is an idea model for studying permeation and of adverse effects on cell walls such as lung and blood capillary walls. As noted above, no studies are as yet available in the areas outlined here on well defined systems. In addition, the effects on electrical properties of such toxic, gaseous compounds will simultaneously be interpreted (electrical resistance and capacitance); this will yield further information on adverse effects of such substances with regard to the functioning of the lung.